1. Taurine-Upregulated Gene 1 Attenuates Cerebral Angiogenesis following Ischemic Stroke in Rats.
- Author
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Li, Fei, Yu, Jun-Hua, Jiang, Hong-Xiang, Zhang, Hui-Kai, Cai, Qiang, Liu, Zai-Ming, Li, Ming-Chang, and Chen, Qian-Xue
- Subjects
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BIOLOGICAL models , *REVERSE transcriptase polymerase chain reaction , *ANIMAL behavior , *STATISTICS , *NEOVASCULARIZATION , *ISCHEMIC stroke , *ANIMAL experimentation , *IMMUNOHISTOCHEMISTRY , *WESTERN immunoblotting , *ONE-way analysis of variance , *MICRORNA , *RATS , *GENE expression , *BIOINFORMATICS , *NEUROPSYCHOLOGICAL tests , *T-test (Statistics) , *DESCRIPTIVE statistics , *VASCULAR endothelial growth factors , *T cells , *DATA analysis software , *DATA analysis - Abstract
Objective. Angiogenesis is one of the therapeutic targets of cerebral infarction. Long noncoding RNAs (lncRNAs) can regulate the pathological process of angiogenesis following ischemic stroke. Taurine-upregulated gene 1 (TUG1), an lncRNA, is correlated to ischemic stroke. We intended to determine the effect of TUG1 on angiogenesis following an ischemic stroke. Materials and Methods. Middle cerebral artery occlusion (MCAO) was adopted to build a focal ischemic model of the rat brain, and pcDNA-TUG1 and miR-26a mimics were injected into rats. Neurological function was estimated through modified neurological severity scores. The volume of focal brain infarction was calculated through 2,3,5-triphenyltetrazolium chloride staining. The level of TUG1 and miR-26a was measured by PCR. The expression of vascular endothelial growth factor (VEGF) and CD31 was checked using immunohistochemistry and western blot. The correlation between miR-26a and TUG1 was verified through a luciferase reporter assay. Results. TUG1 increased noticeably while miR-26a was markedly reduced in MCAO rats. Overexpression of miR-26a improved neurological function recovery and enhanced cerebral angiogenesis in MCAO rats. TUG1 overexpression aggravated neurological deficits and suppressed cerebral angiogenesis in MCAO rats. Bioinformatics analysis revealed that miR-26a was one of the predicted targets of TUG1. Furthermore, TUG1 combined with miR-26a to regulate angiogenesis. TUG1 overexpression antagonized the role of miR-26a in neurological recovery and angiogenesis in MCAO rats. Conclusions. TUG1/miR-26a, which may act as a regulatory axis in angiogenesis following ischemic stroke, can be considered a potential target for cerebral infarction therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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